4.5 Article

The anti-inflammatory peptide Catestatin blocks chemotaxis

Journal

JOURNAL OF LEUKOCYTE BIOLOGY
Volume 112, Issue 2, Pages 273-278

Publisher

OXFORD UNIV PRESS
DOI: 10.1002/JLB.3CRA1220-79ORR

Keywords

catestatin; chemotaxis; M phi s; migration; monocytes; neutrophil; pro-angiogenesis

Funding

  1. Human Frontier Science Program (HFSP) [RGY0080/2018]
  2. Netherlands Organization for Scientific Research [NWO-ALWVIDI 864.14.001]
  3. European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program [862137]
  4. US Department of Veterans Affairs [I01BX000323]
  5. Swedish Research Council
  6. Swedish Society for Medical Research
  7. Goran Gustafsson foundation
  8. EMBO fellowship [EMBO7887]

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Increased levels of the anti-inflammatory peptide Catestatin (CST) correlate with less severe outcomes in hypertension, colitis, and diabetes, partly due to its regulation of chemotaxis, which reduces the infiltration of monocytes and macrophages in inflamed tissues.
Increased levels of the anti-inflammatory peptide Catestatin (CST), a cleavage product of the pro-hormone chromogranin A, correlate with less severe outcomes in hypertension, colitis, and diabetes. However, it is unknown how CST reduces the infiltration of monocytes and macrophages (M phi s) in inflamed tissues. Here, it is reported that CST blocks leukocyte migration toward inflammatory chemokines. By in vitro and in vivo migration assays, it is shown that although CST itself is chemotactic, it blocks migration of monocytes and neutrophils to inflammatory attracting factor CC-chemokine ligand 2 (CCL2) and C-X-C motif chemokine ligand 2 (CXCL2). Moreover, it directs CX(3)CR1(+) M phi s away from pancreatic islets. These findings suggest that the anti-inflammatory actions of CST are partly caused by its regulation of chemotaxis.

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